1) COVID-19: A DISEASE OF TRANSCRIPTIONAL ERROR - EPIGENETICS

COVID-19 is without question a multi-systemic syndrome like no other with vast variance and involvement. I believe we are viewing the disease incorrectly. COVID-19 is unique. Instead of the DISEASE causing PATHOLOGY,
2) the DISEASE dysregulates TRANSCRIPTION causing the HOST to cause PATHOLOGY.

It is the only logical conclusion I can arrive at given the unprecedented panoply of systemic involvement and symptoms, and how UNIQUE it ultimately is, to each host.

Many different diseases and
3) syndromes, including cancer, autoimmunity, neurological disorders, diabetes, cardiovascular disease, and obesity, can be caused by mutations in regulatory sequences and in the transcription factors, cofactors, chromatin regulators, and noncoding RNAs that interact with these
4) regions.

What is most interesting is that it is now understood that a small fraction of the hundreds of transcription factors that are present dominate the control of much of the active gene expression program.

The Spike Protein not only binds to Ace-2, but it also, like a
5) droid, "hacks" its vast transcription network.

A transcription regulatory network within the ACE2 locus may promote a pro-viral environment for SARS-CoV-2 by modulating expression of host factors.

cell.com/fulltext/S0092…

biorxiv.org/content/10.110…
THIS IS WHY COVID-19 BEARS SUCH SIMILARITY TO LUNG CANCER AND AUTOIMMUNE DISEASES. BECAUSE THE HOST IS BEING "INSTRUCTED" TO CAUSE THE DISEASE. PRECISELY THE SAME WAY CANCER AND AUTOIMMUNE DISEASES DO.

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More from @Parsifaler

6 Jul
1) There appears to be an intimate associate between the spike protein and clotting. Especially microclotting, which has been obeserved in the alveoli of severe covid. There have been strokes and heart attacks even in asymptomatic cases.

However, what are the mechanisms Image
2) of this connection? One very important clue is the role of Interstitial Lung Disease. The spike protein has been proven to cause synctia in the lung. Patients showed extensive blood clotting of the lung arteries and veins (thrombosis). Second, several lung cells were
3) abnormally large and had many nuclei, resulting from the fusion of different cells into single large cells. This formation of fused cells (syncytia) is due to the viral spike protein, which the virus uses to enter the cell. When the protein is present on the surface of cells
Read 8 tweets
5 Jul
1) MOLECULAR MIMICRY AND THE MICROBIOME APPROACH (NOT JUST GUT MICROBIOME, BACTERIA ARE UBIQUITOUS IN THE BODY), SARS-CoV-2 IS A BACTERIOPHAGE:

It appears to be increasingly apparent that metabolism and transcription dysregulation are front and center in COVID-19. It could be Image
2) that there is a "CO-CONSPIRATOR" in the body of those who suffer from severe disease and death. For example, cross-reactions with H. Pylori alone can trigger idiopathic thrombocytopenic purpura. There may be unidentified bacteria that SARS-CoV-2 is infecting in the body, Image
causing much of this dysregulation. Please watch the referenced video. It is extremely important.

journals.lww.com/co-rheumatolog…

pubmed.ncbi.nlm.nih.gov/32358202/

ncbi.nlm.nih.gov/pmc/articles/P…

Image
Read 7 tweets
2 Jul
1) LKB1, MASTER COVID SPECTRE: FROM CARCINOGENESIS TO METABOLISM, AM DYSFUNCTION AND SKELETAL MUSCLE HOMEOSTASIS

I believe without question the spike protein is downregulating/"turning off" expression of LKB1. At first glance, the most immediate danger is carcinogenesis
2) as it was found that loss of Lkb1 was sufficient to drive the initial steps of carcinogenesis ex vivo.

Lkb1 plays an important role in regulating glucose homeostasis and energy metabolism. In addition, there is also evidence that has highlighted a prominent role for Lkb1 in
3) the function of macrophages. Lkb1 inhibits the activation and inflammatory function of innate macrophages. It was found that disruption of Lkb1 impaired the self-renewal of AMs, contributing to the reduction of AMs, which led to aggravated symptoms and EXCESSIVE accumulation
Read 9 tweets
2 Jul
1) METABOLICALLY INDUCED IMMUNE DEFICIENCY

Given the mitcochondrial dysfunction obeserved in COVID-19, I have turned my attention towards liver kinase B1 (LKB1). This kinase is intimately involved with both ATP production, T-cell development, peripheral T-cell homeostasis, and
2) T-cell effector function.

I believe SARS-CoV-2 is epigenetically impairing LKB1. LKB1-deficient T cells exhibited defects in cell proliferation and viability and altered glycolytic and lipid metabolism. Interestingly, loss of LKB1 promoted increased T cell activation and
3) inflammatory cytokine production by both CD4+ and CD8+ T cells.

LKB1 was recently found to have prominent roles in hematopoietic stem cell viability and renewal, suggesting a prominent function for LKB1 in hematopoietic cells. These features are also observed in COVID-19.
Read 8 tweets
1 Jul
1) LKB1: THE STAR OF THE SHOW IS STILL WAITING IN THE WINGS: HOW HAVE WE MISSED THIS?

Endothelial Cell-Specific LKB1 Deletion Causes Endothelial Dysfunction and Hypertension in Mice in vivo

The gene, also known as STK11, is involved in controlling blood sugar levels.

LKB1
2) programs the metabolic and functional fitness of Treg cells in the control of immune tolerance and homeostasis. Mice with a Treg-specific deletion of LKB1 developed a fatal inflammatory disease characterized by excessive TH2-type-dominant responses. LKB1 deficiency disrupted
3) Treg cell survival and mitochondrial fitness and metabolism, but also induced aberrant expression of immune regulatory molecules including the negative co-receptor PD-1 and the TNF receptor superfamily proteins GITR and OX40. The results point to functional exhaustion of Treg
Read 9 tweets
30 Jun
1) ARE REGULATORY T CELLS BEING EXHAUSTED BY EXPOSURE TO THE SPIKE PROTEIN SUPERALLERGEN IN SEVERE COVID?

There has been much discussion of immune dysregulation in COVID-19 disease. One of the most interesting recurring findings is CD8 T-Cell Exhaustion. CD8 T-Cells are
2) regulatory T-cells. What is most curious is that they become MORE exhausted the MORE severe the disease is.

I believe this is due to the increased presence and persistence of SPIKE PROTEINS.

If you look at LKB1, this liver kinase allows access to CHROMATIN (regulates
3) METASTASIS), MITOCHONDRIAL FUNCTION and T-REGS.

Spike Protein sequences interact with WIPI3/WDR45B. which are scaffolds of the LKB1 signalling circuits.

This may offer evidence that prolonged exposure to the spike protein is behind the allergic/superallergen nature of
Read 11 tweets

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